-
摘要: EB病毒（Epstein-Barr virus，EBV）是最早被确定的人类肿瘤病毒，在人群中广泛传播，感染呈多样性。EBV与伯基特淋巴瘤、霍奇金淋巴瘤等多种淋巴瘤以及鼻咽癌、胃癌等多种实体肿瘤相关，还能引起移植后淋巴增生性疾病和自身免疫病等多种疾患。EBV以隐性感染的方式终身潜伏，在少数免疫力低下者体内通过多种途径在多种疾病中起作用，或与其他因素协同作用导致复杂疾病，可能与多种疑难病症相关，引起了临床研究者的关注。虽然已有一些抗人类疱疹病毒的药物用于临床，但是对于EBV感染无效，抗EBV感染的药物和疫苗正在积极研究中。对EBV感染多样性的研究不仅有临床意义，也为微进化规律的研究提供新线索。Abstract: The Epstein-Barr virus (EBV) is the first identified human tumor virus. EBV infection is widely spread in the population and has diverse manifestations. EBV infection is associated with many types of lymphoma, including Burkitt's lymphoma and Hodgkin's lymphoma, as well as solid tumors, including nasopharyngeal carcinoma and gastric cancer. It can also cause lymphoproliferative and autoimmune diseases in patients who have undergone organ transplantation. EBV is retained in the body in a latent form. In patients with impaired immunity, EBV infection is involved in multiple diseases or interacts with other factors to lead to complex and potentially refractory diseases. These phenomena have attracted the attention of clinical researchers. Although some anti-herpes virus drugs have been used in clinical practice, they are not effective against EBV infection; more drugs and vaccines are being actively studied. Study of the diversity in EBV infections has clinical significance; furthermore, it provides clues for the study of microevolution.
-
图 1 EBV的生活周期
EBV初始感染（通常由唾液传染）后建立双相的生活周期：在免疫监督下维持不产生病毒颗粒的基因组，称为隐性周期；初始感染或免疫抑制状况下细胞融解产生有感染性病毒颗粒的感染性融解周期。EBV在不同细胞和B细胞的不同分化阶段导致不同的隐性感染类型。EA-早期抗原；EBER-EBV编码的小RNA；EBNA-EBV核抗原；LMP-晚期膜抗原；VCA-病毒壳抗原
表 2 慢性EBV感染的相关综合征
表 3 EBV感染血清学试验的临床意义
表 4 EBV引起的代谢变化[16]
-
[1] 吴克复, 马小彤, 郑国光, 等. 疱疹病毒隐性感染的机制及意义[J]. 白血病•淋巴瘤, 2018, 27(5): 257-261. [2] 吴克复, 郑国光, 马小彤, 等. B细胞淋巴瘤的细胞组成及其作用[J]. 白血病·淋巴瘤, 2020, 29(6): 321-325. doi: 10.3760/cma.j.cn115356-20200420-00099 [3] Abbott RJ, Pachnio A, Pedroza-Pacheco I, et al. Asymptomatic primary infection with Epstein- Barr virus: Observations on young adult cases[J]. J Virol, 2017, 91(21): e00382-17. http://europepmc.org/articles/PMC5640854/ [4] Dunmire SK, Verghese PS, Balfour HH. Primary Epstein-Barr virus infection[J]. J Clin Virol, 2018, 102: 84-92. doi: 10.1016/j.jcv.2018.03.001 [5] Baldanti F, Gatti M, Furione M, et al. Kinetics of Epstein-Barr virus DNA load in different blood compartments of pediatric recipients of T-cell-depleted HLA-haploidentical stem cell transplantation[J]. J Clin Microbiol, 2008, 46(11): 3672-3677. doi: 10.1128/JCM.00913-08 [6] Burns DM, Rana S, Martin E, et al. Greatly reduced risk of EBV reactivation in rituximab-experienced recipients of alemtuzumab-conditioned allogeneic HSCT[J]. Bone Marrow Transplant, 2016, 51(6): 825-832. doi: 10.1038/bmt.2016.19 [7] Morscio J, Tousseyn T. Recent insights in the pathogenesis of posttransplantation lymphoproliferative disorders[J]. World J Transplant, 2016, 6(3): 505-516. doi: 10.5500/wjt.v6.i3.505 [8] Andrei G, Trompet E, Snoeck R. Novel therapeutics for Epstein(-) Barr virus[J]. Molecules, 2019, 24(5): 997. doi: 10.3390/molecules24050997 [9] Iizasa H, Ishihara S, Richardo T, et al. Dysbiotic infection in the stomach [J]. World J Gastroenterol, 2015 21(40): 11450-11457. doi: 10.3748/wjg.v21.i40.11450 [10] Kimura H. EBV in T-/NK-cell tumorigenesis[J]. Adv Exp Med Biol, 2018, 1045: 459-475. doi: 10.1007/978-981-10-7230-7_21 [11] Kimura H, Cohen JI. Chronic active Epstein-Barr virus disease[J]. Front Immunol, 2017, 8: 1867. doi: 10.3389/fimmu.2017.01867 [12] Pandey S, Jha HC, Shukla SK, et al. Epigenetic regulation of tumor suppressors by helicobacter pylori enhances EBV-induced proliferation of gastric epithelial cells[J]. mBio, 2018, 9(2): e00649-18. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5915740/ [13] Shannon-Lowe C, Rickinson AB, Bell AI. Epstein-Barr virus-associated lymphomas[J]. Philos Trans R Soc Lond B Biol Sci, 2017, 372(1732): 20160271. doi: 10.1098/rstb.2016.0271 [14] Worth AJ, Houldcroft CJ, Booth C. Severe Epstein-Barr virus infection in primary immunodeficiency and the normal host[J]. Br J Haematol, 2016, 175(4): 559-576. doi: 10.1111/bjh.14339 [15] Kimura H, Fujiwara S. Overview of EBV-associated T/NK-cell lymphoproliferative diseases[J]. Front Pediatr, 2018, 6: 417. http://www.researchgate.net/publication/330140864_Overview_of_EBV-Associated_TNK-Cell_Lymphoproliferative_Diseases [16] Lo AK, Dawson CW, Young LS, et al. The role of metabolic reprogramming in gamma- herpesvirus- associated oncogenesis[J]. Int J Cancer, 2017, 141(8): 1512-1521. doi: 10.1002/ijc.30795 [17] Dreyfus DH. Gene sharing between Epstein-Barr virus and human immune response genes[J]. Immunol Res, 2017, 65(1): 37-45. doi: 10.1007/s12026-016-8814-x [18] Fierz W. Multiple sclerosis: an example of pathogenic viral interaction [J]? Virol J, 2017, 14(1): 42. http://www.ncbi.nlm.nih.gov/pubmed/28241767/ [19] Fernandez-Menendez S, Fernandez-Moran M, Fernandez-Vega I, et al. Epstein-Barr virus and multiple sclerosis. From evidence to therapeutic strategies[J]. J Neurol Sci, 2016, 361: 213-219. http://search.ebscohost.com/login.aspx?direct=true&db=aph&AN=112472669&site=ehost-live [20] Laurence M, Benito-Leon J. Epstein-Barr virus and multiple sclerosis: Updating pender's hypothesis[J]. Mult Scler Relat Disord, 2017, 16: 8-14. doi: 10.1016/j.msard.2017.05.009 [21] Minarovits J, Niller HH. Current trends and alternative scenarios in EBV research[J]. Methods Mol Biol, 2017, 1532: 1-32. http://www.ncbi.nlm.nih.gov/pubmed/27873264 [22] Sanjuan R. Collective properties of viral infectivity[J]. Curr Opin Virol, 2018, 33: 1-6. doi: 10.1016/j.coviro.2018.06.001 [23] Elgui de Oliveira D, Muller-Coan BG, Pagano JS. Viral carcinogenesis beyond malignant transformation: EBV in the progression of human cancers[J]. Trends Microbiol, 2016, 24(8): 649-664. doi: 10.1016/j.tim.2016.03.008 [24] Murray PG, Young LS. An etiological role for the Epstein-Barr virus in the pathogenesis of classical Hodgkin lymphoma[J]. Blood, 2019, 134 (7): 591-596. doi: 10.1182/blood.2019000568 [25] Miller IJ. Epstein Barr virus infection can be a secondary event in B-cell lymphomas: A review of 338 cases and a novel finding of zonal EBER+ tumor cells showing features of progression from underlying EBVnegative lymphoma[J]. Appl Immunohistochem Mol Morphol, 2019, 27(3): 165-173. doi: 10.1097/PAI.0000000000000562 [26] Stamatiou DP, Derdas SP, Zoras OL, et al. Herpes and polyoma family viruses in thyroid cancer[J]. Oncol Lett, 2016, 11(3): 1635-1644. doi: 10.3892/ol.2016.4144 [27] Kerr JR. Epstein-Barr virus (EBV) reactivation and therapeutic inhibitors [J]. J Clin Pathol, 2019, 72(10): 651-658. doi: 10.1136/jclinpath-2019-205822 [28] Cohen JI, Fauci AS, Varmus H, et al. Epstein-Barr virus: an important vaccine target for cancer prevention[J]. Sci Transl Med, 2011, 3(107): 107fs7. http://europepmc.org/articles/PMC3501269 [29] Cohen JI. Epstein-barr virus vaccines[J]. Clin Transl Immunology, 2015, 4(1): e32. doi: 10.1038/cti.2014.27 [30] Cohen, JI. Vaccine development for Epstein-Barr virus[J]. Adv Exp Med Biol, 2018, 1045: 477-493. http://europepmc.org/abstract/MED/29896681 [31] 吴克复, 郑国光, 马小彤, 等. 白血病病毒病因的现代观[J]. 中国肿瘤临床, 2018, 45(7): 325-330. doi: 10.3969/j.issn.1000-8179.2018.07.072 [32] 吴克复, 马小彤, 郑国光, 等. 非细胞病原体(纳米病原体)及其致病作用[J]. 医学研究杂志, 2019, 48(6): 1-6. https://www.cnki.com.cn/Article/CJFDTOTAL-YXYZ201906003.htm [33] 吴克复, 郑国光, 许子亮, 等. 微进化与现代病－现代病的进化原理[M]. 北京: 科学出版社, 2020. -
下载:
点击查看大图
图(2) / 表(4)
计量
- 文章访问数: 235
- HTML全文浏览量: 11
- PDF下载量: 96
- 被引次数: 0
